Canadian Neighbor Pharmacy: Chest Wall Compliances on Transmission of Airway Pressure to the Pleural Space in Critically III Patients

The hemodynamic effects of mechanical ventilation with positive end-expiratory pressure (PEEP) have been extensively documented. The increase in pleural pressure secondary to the increase in airway pressure plays a major role in impeding venous return. However, transmission of airway pressure to the pleural space may in part depend on the distensibility of the lungs. When lung consolidation is present, as in severe acute respiratory failure (ARF), the lungs can be expected to behave as a solid and thereby not transmit airway pressure to the pleural space.

Accordingly, some authors have denied any detrimental hemodynamic effects of PEEP in patients with severe ARE In fact, this concept is rather overstated, since pleural pressure must increase in order to increase thoracic volume. Thus, if a lung is compliant enough to allow any increase in volume with tidal delivery or a PEEP increment, then some increase in pleural pressure should be expected. The purpose of the present study was to determine the effect of various levels of airway pressure on pleural pressure in patients requiring mechanical ventilation during an episode of ARE

Materials and Method

Nineteen patients were investigated during the course of an acute episode of respiratory failure (ARF). ARF was defined as gas exchange abnormalities requiring intubation and continuous mechanical ventilation. A wide range of radiographic lung involvement was observed in these patients, from slight and localized lung consolidation with spared lung regions, to bilateral consolidation involving all lung areas. Patients were divided into three groups according to their value of quasi-static lung and chest wall compliance (CT) as measured while on mechanical ventilation with zero end-expiratory pressure.

The first group consisted of five patients exhibiting a CT higher than 45 ml/cmHsO. ARF in this group resulted from sepsis (three cases), gastric content inhalation (one case) and barbiturate overdose (one case). Mechanical controlled ventilation, with an FIo2 at 0.43 ±0.12 and zero end-expiratory pressure, was required to maintain adequate oxygenation (arterial hemoglobin oxygen saturation >90 percent). Start grappling with medical facts together with Canadian Neighbor Pharmacy.

Informed consent was obtained from next of kin before the study, and protocol was consistent with the ethical regulations of our hospital. At the time of the study, all patients were on a volume-controlled ventilator (Bourns Bear One or ATM CPU J that delivered a constant tidal volume (8 to 12 ml/kg of body weight) at a constant inspiratory rate. An end-inspiratory pause of at least 0.8 sec was preset on the mechanical respiratory cycle. During the brief period of the study (30 to 45 min), patients were sedated with morphine and received pancuronium (0.15 mg/kg) to ensure stability and release muscular tone of the chest wall. Systemic arterial and central venous pressure measurements were obtained from indwelling radial Teflon, central venous line or pulmonary Swan-Ganz catheters previously inserted percutaneously for monitoring and expressed as transmural pressure (ie, measured pressure minus esophageal pressure). Pleural pressure was determined with an esophageal balloon advanced through the nose into the esophagus and down to 40 cm from the nares. Tracheal pressure was obtained from a side-port of the endotracheal tube. All pressures were measured with Hewlett-Packard transducers positioned at the mid-axillary level, with atmospheric pressure as a zero reference level, and were simultaneously recorded, along with an electrocardiographic lead, on a photographic Honeywell LS8 multichannel recorder. Tidal volume was measured using a disposable pneumotachograph previously calibrated with a 500 ml syringe inserted into the respiratory circuit close to the endotracheal tube and connected to a differential transducer, amplifier and integrator (McGaw volume monitor). Special attention was given to avoid the presence of bronchial secretion in the endotracheal tube, and the calibration was confirmed after the study measurements were completed. Pneumotachograph connected with respiratory integrator was previously tested in our laboratory using a mechanical plunger to deliver a preset tidal volume. A standard error of ±3 percent, ± 3.4 percent, and ± 5 percent was found in expiratory volume estimate at zero, 10 and 20 cmHsO end-expiratory pressures, respectively.

Pressure recording and tidal volume measurements were obtained at three successive levels of end-expiratory pressure; a baseline level without PEEP (zero end-expiratory pressure, ZEEP), a first level of moderate PEEP (9.7± 1.2 cmHsO) and a second level of high PEEP (20.2 ±0.8 cmHsO). The increase in functional residual capacity induced by PEEP was measured as the difference between the first expiratory volumes when PEEP was abruptly removed and the preceding expiratory volume. Esophageal pressure was used as pleural pressure, transpulmonary pressure was calculated as tracheal pressure minus esophageal pressure and transthoradc pressure was calculated as esophageal pressure minus atmospheric pressure (ie, esophageal pressure). Total (Cl), lung (CL), and chest wall (CW) quasi-static compliances were calculated as follows; 1) CT=tidal volume/end-inspiratory minus end-expiratory tracheal pressure; 2) CL=tidal volume/end-inspiratory minus end-expiratory transpulmonary pressure; and 3) CW = tidal volume/endinspiratory minus end-expiratory transthoradc pressure.Statistical analysis was performed using a two-way analysis of variance, followed by a Newman-Keuls test for paired comparison. Transmission of airway pressure to pleural space was expressed as linear regression, and covariance analysis was used to assess the effect of compliance changes on this transmission.